Outline

Background: Air pollution has been associated with cardiovascular disease exacerbation in numerous studies. The mechanisms linking the inhalation of ambient particles to adverse cardiovascular events are not completely understood. Based on previous findings, we hypothesised that particulate air pollution might induce systemic inflammation in myocardial infarction (MI) survivors, a particularly vulnerable group.

Materials and Methods: A prospective longitudinal study of 1,003 MI survivors was performed in six cities between May 2003 and July 2004. Repeated measurements (average 5.8 per patient) of IL-6, fibrinogen and C-reactive protein (CRP) were compared to concurrent levels of air pollution. Hourly data on particle number concentrations (PNC), mass concentrations of less than 10 Âµm (PM10) and 2.5 Âµm (PM2.5) and meteorological data were collected at central monitoring sites in each city. City specific confounder models were built for each blood marker separately adjusting for meteorology and time-invariant covariates. Data were analyzed with mixed effects models.

Results: Pooled results show an increase in IL-6 when concentrations of PNC were elevated 12-17 hours before blood withdrawal [%change of geometric mean: 2.7, CI:1.0;4.6]. Five day cumulative exposure to PM10 was associated with increased fibrinogen concentrations [%change of arithmetric mean: 0.6, CI:0.1;1.1]. Results on PM10 were similar among non-smokers, patients with elevated levels of N-Terminal proB-type natriuretic peptide and HbA1c, used as indicators for left ventricular dysfunction and hyperglycaemia, respectively [%change of arithmetric mean: 1.03, CI:0.16;1.90, 0.70, CI:-0.02;1.42 and 1.92, CI:0.60;3.24, respectively]. No consistent associations were found for CRP.

Conclusion: To our knowledge no epidemiological study on air pollution of this size using repeated measurements has been conducted. Results indicate an immediate response to PNC on the IL-6 level, possibly leading to the production of acute phase proteins, as seen in slightly increased fibrinogen levels. This might provide a link between air pollution and adverse cardiac events.